| Human mesenchymal stem cells suppress chronic airway inflammation in the murine ovalbumin asthma model. | |
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MedLine Citation:
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PMID: 20817776 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Allogeneic human mesenchymal stem cells (hMSCs) introduced intravenously can have profound anti-inflammatory activity resulting in suppression of graft vs. host disease as well as regenerative events in the case of stroke, infarct, spinal cord injury, meniscus regeneration, tendinitis, acute renal failure, and heart disease in human and animal models of these diseases. hMSCs produce bioactive factors that provide molecular cuing for: 1) immunosuppression of T cells; 2) antiscarring; 3) angiogenesis; 4) antiapoptosis; and 5) regeneration (i.e., mitotic for host-derived progenitor cells). Studies have shown that hMSCs have profound effects on the immune system and are well-tolerated and therapeutically active in immunocompetent rodent models of multiple sclerosis and stroke. Furthermore, intravenous administration of MSCs results in pulmonary localization. Asthma is a major debilitating pulmonary disease that impacts in excess of 150 million people in the world with uncontrolled asthma potentially leading to death. In addition, the socioeconomic impact of asthma-associated illnesses at the pediatric and adult level are in the millions of dollars in healthcare costs and lost days of work. hMSCs may provide a viable multiaction therapeutic for this inflammatory lung disease by secreting bioactive factors or directing cellular activity. Our studies show the effectiveness and specificity of the hMSCs on decreasing chronic airway inflammation associated with the murine ovalbumin model of asthma. In addition, the results from these studies verify the in vivo immunoeffectiveness of hMSCs in rodents and support the potential therapeutic use of hMSCs for the treatment of airway inflammation associated with chronic asthma. |
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Authors:
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Tracey L Bonfield; Mary Koloze; Donald P Lennon; Brandon Zuchowski; Sung Eun Yang; Arnold I Caplan |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-09-03 |
Journal Detail:
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Title: American journal of physiology. Lung cellular and molecular physiology Volume: 299 ISSN: 1522-1504 ISO Abbreviation: Am. J. Physiol. Lung Cell Mol. Physiol. Publication Date: 2010 Dec |
Date Detail:
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Created Date: 2010-12-06 Completed Date: 2011-01-13 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 100901229 Medline TA: Am J Physiol Lung Cell Mol Physiol Country: United States |
Other Details:
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Languages: eng Pagination: L760-70 Citation Subset: IM |
Affiliation:
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Dept. of Pediatrics, Case Western Reserve Univ., Cleveland, OH 44106-4948, USA. tracey.bonfield@case.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adult Animals Asthma / chemically induced*, immunology, pathology, therapy* Child Cytokines / immunology Disease Models, Animal Humans Immunoglobulin E / blood Interferon-gamma / immunology Interleukin-1beta / immunology Mesenchymal Stem Cell Transplantation / methods* Mesenchymal Stem Cells / immunology* Mice Mice, Inbred BALB C Nitric Oxide / metabolism Ovalbumin / pharmacology* Pneumonia / chemically induced*, immunology, pathology, therapy* |
| Chemical | |
Reg. No./Substance:
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0/Cytokines; 0/Interleukin-1beta; 10102-43-9/Nitric Oxide; 37341-29-0/Immunoglobulin E; 82115-62-6/Interferon-gamma; 9006-59-1/Ovalbumin |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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